Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury
Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated a...
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| Published in | eLife Vol. 5; p. e12661 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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England
eLife Science Publications, Ltd
19.04.2016
eLife Sciences Publications Ltd eLife Sciences Publications, Ltd |
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| Abstract | Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury. |
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| AbstractList | Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury. Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury. Around 20% of the world’s population experiences long-lasting “chronic” pain, which often results in poor sleep, depression and anxiety. One of the most disabling forms of chronic pain is called neuropathic pain, which results from injuries to sensory nerves. Pain or discomfort is felt in response to touches that are not normally painful. Neuropathic pain is difficult to treat as we do not fully understand the molecular mechanisms that cause it. Stimulating a nerve causes it to produce action potentials. At a molecular level, these action potentials are generated by ions moving into and out of the neuron through proteins called ion channels. The movement of sodium ions into a neuron triggers an action potential, and the movement of potassium ions out of the neuron returns it to a resting state. After a sensory nerve is cut or otherwise damaged it becomes hyperactive and produces spontaneous electrical activity that the brain interprets as pain signals. However, it is not fully understood how cutting a nerve affects the ion channels in a way that generates this hyperactivity. Different types of ion channel are found in different regions of the nerve cell; for example, type 1 potassium channels are normally found in a region called the juxtaparanode at the axon of the neuron. Calvo et al. have now tracked what happens to type 1 potassium channels after nerve injury in rats. Soon after nerve damage occurred, nearly all of these ion channels disappeared from the juxtaparanode. At the same time, electrical activity in the cut nerve increased, and the recovering animals responded in ways that suggested they were hypersensitive to the nerve being touched. Three weeks after the injury, most rats lost their hypersensitivity and the electrical activity in the cut nerve returned to near-normal levels. Calvo et al. found that the recovering nerves contained new subtypes of type 1 potassium channels. These potassium channels did not just appear in the juxtaparanode: they also invaded the ‘fence’ region that normally separates potassium channels from sodium channels. The same was observed to happen in the nerves of patients that suffer from neuropathic pain due to a nerve injury. At this late time point after nerve injury, blocking the activity of potassium channels produced the same abnormal increase in the nerve’s electrical activity as seen immediately after the nerve had been cut. The rats’ hypersensitivity to touch also returned. This suggests that the appearance of the new potassium channel subtypes might be a protective mechanism that reduces the activity of a damaged nerve to decrease pain. These findings suggest new ways of treating neuropathic pain. Further studies are now needed to investigate whether drugs that can activate the new potassium channel subtypes could stop pain from an injured nerve becoming a long-term problem. Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury. DOI: eLife digest Around 20% of the world's population experiences long-lasting "chronic" pain, which often results in poor sleep, depression and anxiety. One of the most disabling forms of chronic pain is called neuropathic pain, which results from injuries to sensory nerves. Pain or discomfort is felt in response to touches that are not normally painful. Neuropathic pain is difficult to treat as we do not fully understand the molecular mechanisms that cause it. Stimulating a nerve causes it to produce action potentials. At a molecular level, these action potentials are generated by ions moving into and out of the neuron through proteins called ion channels. The movement of sodium ions into a neuron triggers an action potential, and the movement of potassium ions out of the neuron returns it to a resting state. After a sensory nerve is cut or otherwise damaged it becomes hyperactive and produces spontaneous electrical activity that the brain interprets as pain signals. However, it is not fully understood how cutting a nerve affects the ion channels in a way that generates this hyperactivity. Different types of ion channel are found in different regions of the nerve cell; for example, type 1 potassium channels are normally found in a region called the juxtaparanode at the axon of the neuron. Calvo et al. have now tracked what happens to type 1 potassium channels after nerve injury in rats. Soon after nerve damage occurred, nearly all of these ion channels disappeared from the juxtaparanode. At the same time, electrical activity in the cut nerve increased, and the recovering animals responded in ways that suggested they were hypersensitive to the nerve being touched. Three weeks after the injury, most rats lost their hypersensitivity and the electrical activity in the cut nerve returned to near-normal levels. Calvo et al. found that the recovering nerves contained new subtypes of type 1 potassium channels. These potassium channels did not just appear in the juxtaparanode: they also invaded the 'fence' region that normally separates potassium channels from sodium channels. The same was observed to happen in the nerves of patients that suffer from neuropathic pain due to a nerve injury. At this late time point after nerve injury, blocking the activity of potassium channels produced the same abnormal increase in the nerve's electrical activity as seen immediately after the nerve had been cut. The rats' hypersensitivity to touch also returned. This suggests that the appearance of the new potassium channel subtypes might be a protective mechanism that reduces the activity of a damaged nerve to decrease pain. These findings suggest new ways of treating neuropathic pain. Further studies are now needed to investigate whether drugs that can activate the new potassium channel subtypes could stop pain from an injured nerve becoming a long-term problem. DOI: Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury.DOI: http://dx.doi.org/10.7554/eLife.12661.001 Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of shaker-type-potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury. DOI: http://dx.doi.org/10.7554/eLife.12661.001 Around 20% of the world’s population experiences long-lasting “chronic” pain, which often results in poor sleep, depression and anxiety. One of the most disabling forms of chronic pain is called neuropathic pain, which results from injuries to sensory nerves. Pain or discomfort is felt in response to touches that are not normally painful. Neuropathic pain is difficult to treat as we do not fully understand the molecular mechanisms that cause it. Stimulating a nerve causes it to produce action potentials. At a molecular level, these action potentials are generated by ions moving into and out of the neuron through proteins called ion channels. The movement of sodium ions into a neuron triggers an action potential, and the movement of potassium ions out of the neuron returns it to a resting state. After a sensory nerve is cut or otherwise damaged it becomes hyperactive and produces spontaneous electrical activity that the brain interprets as pain signals. However, it is not fully understood how cutting a nerve affects the ion channels in a way that generates this hyperactivity. Different types of ion channel are found in different regions of the nerve cell; for example, type 1 potassium channels are normally found in a region called the juxtaparanode at the axon of the neuron. Calvo et al. have now tracked what happens to type 1 potassium channels after nerve injury in rats. Soon after nerve damage occurred, nearly all of these ion channels disappeared from the juxtaparanode. At the same time, electrical activity in the cut nerve increased, and the recovering animals responded in ways that suggested they were hypersensitive to the nerve being touched. Three weeks after the injury, most rats lost their hypersensitivity and the electrical activity in the cut nerve returned to near-normal levels. Calvo et al. found that the recovering nerves contained new subtypes of type 1 potassium channels. These potassium channels did not just appear in the juxtaparanode: they also invaded the ‘fence’ region that normally separates potassium channels from sodium channels. The same was observed to happen in the nerves of patients that suffer from neuropathic pain due to a nerve injury. At this late time point after nerve injury, blocking the activity of potassium channels produced the same abnormal increase in the nerve’s electrical activity as seen immediately after the nerve had been cut. The rats’ hypersensitivity to touch also returned. This suggests that the appearance of the new potassium channel subtypes might be a protective mechanism that reduces the activity of a damaged nerve to decrease pain. These findings suggest new ways of treating neuropathic pain. Further studies are now needed to investigate whether drugs that can activate the new potassium channel subtypes could stop pain from an injured nerve becoming a long-term problem. DOI: http://dx.doi.org/10.7554/eLife.12661.002 |
| Audience | Academic |
| Author | Zhu, Ning McMahon, Stephen B Richards, Natalie Schmid, Annina B Court, Felipe A Calvo, Margarita Bhat, Manzoor A Anwandter, Philipp Barroso, Alejandro Zhu, Lan Ivulic, Dinka Bennett, David L H |
| Author_xml | – sequence: 1 givenname: Margarita orcidid: 0000-0003-3349-9189 surname: Calvo fullname: Calvo, Margarita organization: Departamento de Anestesiologia, Facultad de Medicina, Pontificia Universidad Catolica de Chile, Santiago, Chile – sequence: 2 givenname: Natalie surname: Richards fullname: Richards, Natalie organization: Wolfson Centre for Age-Related Diseases, Kings College London, London, United Kingdom – sequence: 3 givenname: Annina B surname: Schmid fullname: Schmid, Annina B organization: Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom – sequence: 4 givenname: Alejandro surname: Barroso fullname: Barroso, Alejandro organization: Hospital Regional Universitario de Málaga. Servicio de Anestesiología, Málaga, Spain – sequence: 5 givenname: Lan surname: Zhu fullname: Zhu, Lan organization: School of Allied Health Sciences, Faculty of Health and Life Sciences, De Montfort University, Leicester, United Kingdom – sequence: 6 givenname: Dinka surname: Ivulic fullname: Ivulic, Dinka organization: Departamento de Fisiologia, Facultad de Ciencias Biologicas- Pontificia Universidad Catolica de Chile, Santiago, Chile – sequence: 7 givenname: Ning surname: Zhu fullname: Zhu, Ning organization: Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom – sequence: 8 givenname: Philipp surname: Anwandter fullname: Anwandter, Philipp organization: Departamento Ortopedia y Traumatologia, Facultad de Medicina, Pontificia Universidad Catolica de Chile, Santiago, Chile – sequence: 9 givenname: Manzoor A surname: Bhat fullname: Bhat, Manzoor A organization: School of Medicine, UT Health Science Center at San Antonio, San Antonio, United States – sequence: 10 givenname: Felipe A surname: Court fullname: Court, Felipe A organization: Millenium Nucleus for Regenerative Biology, Pontificia Universidad Catolica de Chile, Santiago, Chile – sequence: 11 givenname: Stephen B surname: McMahon fullname: McMahon, Stephen B organization: Wolfson Centre for Age-Related Diseases, Kings College London, London, United Kingdom – sequence: 12 givenname: David L H surname: Bennett fullname: Bennett, David L H organization: Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27033551$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1152/jn.1992.68.3.734 10.1152/jn.1998.79.4.1814 10.1016/j.neuroscience.2003.11.014 10.1212/WNL.47.1.272 10.1152/physrev.1942.22.4.318 10.1002/jnr.22015 10.1038/nm.3978 10.1038/34916 10.1038/nn.3602 10.1016/S1474-4422(14)70251-0 10.1016/j.pain.2014.03.022 10.1016/S0896-6273(00)81049-1 10.1002/(SICI)1097-4598(199904)22:4<502::AID-MUS12>3.0.CO;2-K 10.1523/JNEUROSCI.4778-08.2009 10.1016/j.neuron.2012.12.035 10.1016/S0896-6273(01)00294-X 10.1002/cne.20321 10.7554/eLife.04660 10.1016/0006-8993(85)90771-1 10.1016/j.pain.2010.09.032 10.1002/glia.21188 10.1016/j.pain.2007.06.030 10.1016/0014-4886(81)90271-5 10.1016/j.neuron.2014.12.042 10.1038/350232a0 10.1083/jcb.201308116 10.1016/j.pain.2006.05.028 10.1016/S0304-3959(99)00211-0 10.1016/S0896-6273(01)00296-3 10.1016/j.pain.2005.10.006 10.1038/283570a0 10.1523/JNEUROSCI.19-19-08589.1999 10.1038/284170a0 10.1083/jcb.200305018 10.1016/0304-3959(92)90041-9 10.1016/S0304-3959(99)00219-5 10.1152/jn.1996.75.6.2629 10.1016/S0169-328X(02)00388-1 10.1083/jcb.150.3.657 10.1016/j.expneurol.2007.09.032 10.1523/JNEUROSCI.19-02-00747.1999 10.1073/pnas.231376298 10.1038/nn.3438 10.1523/JNEUROSCI.4118-04.2005 10.1016/S0304-3959(00)00251-7 10.3389/fnmol.2014.00087 10.1016/0304-3940(81)90270-6 10.1093/brain/awp341 10.1073/pnas.0708574104 10.1371/journal.pbio.1000412 10.1074/jbc.M111.219113 10.1016/0304-3959(83)90164-1 10.1097/AJP.0b013e3181ed0823 10.1126/science.290.5489.124 10.3109/08990228809144642 10.1523/JNEUROSCI.20-07-02742.2000 10.1016/B978-0-12-417027-8.00005-2 10.1523/JNEUROSCI.18-01-00036.1998 10.1523/JNEUROSCI.21-19-07568.2001 10.1002/mus.23314 10.1523/JNEUROSCI.21-08-j0002.2001 10.1016/0304-3959(88)90027-9 10.1016/j.neuron.2005.10.019 10.1016/S0041-0101(00)00162-8 10.1113/jphysiol.2011.224212 10.1038/248740a0 |
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| Copyright | COPYRIGHT 2016 eLife Science Publications, Ltd. 2016, Calvo et al. This work is licensed under the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/3.0/ ) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2016, Calvo et al 2016 Calvo et al |
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| Keywords | juxtaparanode neuropathic pain hypersensitivity rat neuroscience shaker type potassium channels neuropathy human |
| Language | English |
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| References | Gu (bib19) 2011; 286 Wall (bib60) 1974; 248 Madrid (bib35) 2009; 29 Everill (bib15) 1998; 79 Thakur (bib56) 2014; 7 England (bib14) 1996; 47 Nguyen (bib37) 1996; 50 Boyle (bib6) 2001; 30 Vabnick (bib59) 1999; 19 Henry (bib24) 2006; 124 Haroutounian (bib22) 2014; 155 Nikolajsen (bib38) 2010; 26 Yang (bib65) 2004; 123 Chiu (bib9) 1980; 284 Ishikawa (bib25) 1999; 22 Xu (bib64) 2015; 21 Liu (bib32) 2000; 85 Fried (bib17) 1988; 6 MacKinnon (bib34) 1991; 350 Amir (bib1) 1999; 19 DeFelipe (bib11) 1991 Wu (bib63) 2001; 21 Kim (bib30) 2002; 105 Han (bib20) 2000; 84 Poliak (bib44) 2003; 162 Tait (bib55) 2000; 150 Amir (bib2) 2005; 25 Kilkenny (bib28) 2010; 8 Shroff (bib53) 2011; 59 Arroyo (bib3) 2004; 479 Gold (bib18) 1996; 75 Utsunomiya (bib58) 2008; 210 Waxman (bib62) 2014; 17 Dyck (bib13) 1985; 340 Roeper (bib48) 1998; 391 Levinson (bib31) 2012; 46 Jan (bib26) 2012; 590 Campbell (bib7) 1988; 32 Zhao (bib69) 2013; 16 Dorsi (bib12) 2008; 134 Young (bib67) 1942; 22 Bhat (bib4) 2001; 30 Harvey (bib23) 2001; 39 Roza (bib49) 2006; 120 Poliak (bib42) 1999; 24 Stokvis (bib54) 2010; 151 Michaelis (bib36) 2000; 20 Finnerup (bib16) 2015; 14 Kim (bib29) 1992; 50 Pillai (bib41) 2009; 87 Scadding (bib50) 1981; 73 Boucher (bib5) 2000; 290 Kajander (bib27) 1992; 68 Yang (bib66) 2007; 104 Poliak (bib43) 2001; 21 Liu (bib33) 2000; 84 Hao (bib21) 2013; 77 Nyström (bib39) 1981; 27 Trimmer (bib57) 2015; 85 Wall (bib61) 1983; 17 Rasband (bib46) 1998; 18 Rasband (bib47) 2001; 98 Pomicter (bib45) 2010; 133 Zhang (bib68) 2013; 203 Chiu (bib10) 2014; 3 Sherratt (bib52) 1980; 283 Park (bib40) 2003; 16 Chang (bib8) 2013; 72 Sherman (bib51) 2005; 48 |
| References_xml | – year: 1991 ident: bib11 contributor: fullname: DeFelipe – volume: 68 start-page: 734 year: 1992 ident: bib27 article-title: Onset of a painful peripheral neuropathy in rat: a partial and differential deafferentation and spontaneous discharge in a beta and a delta primary afferent neurons publication-title: Journal of Neurophysiology doi: 10.1152/jn.1992.68.3.734 contributor: fullname: Kajander – volume: 79 start-page: 1814 year: 1998 ident: bib15 article-title: Morphologically identified cutaneous afferent DRG neurons express three different potassium currents in varying proportions publication-title: Journal of Neurophysiology doi: 10.1152/jn.1998.79.4.1814 contributor: fullname: Everill – volume: 123 start-page: 867 year: 2004 ident: bib65 article-title: Altered expression of potassium channel subunit mRNA and alpha-dendrotoxin sensitivity of potassium currents in rat dorsal root ganglion neurons after axotomy publication-title: Neuroscience doi: 10.1016/j.neuroscience.2003.11.014 contributor: fullname: Yang – volume: 47 start-page: 272 year: 1996 ident: bib14 article-title: Sodium channel accumulation in humans with painful neuromas publication-title: Neurology doi: 10.1212/WNL.47.1.272 contributor: fullname: England – volume: 22 start-page: 318 year: 1942 ident: bib67 article-title: The functional repair of nervous tissue publication-title: Physiological Reviews doi: 10.1152/physrev.1942.22.4.318 contributor: fullname: Young – volume: 87 start-page: 1773 year: 2009 ident: bib41 article-title: Spatiotemporal ablation of myelinating glia-specific neurofascin (Nfasc NF155) in mice reveals gradual loss of paranodal axoglial junctions and concomitant disorganization of axonal domains publication-title: Journal of Neuroscience Research doi: 10.1002/jnr.22015 contributor: fullname: Pillai – volume: 21 start-page: 1326 year: 2015 ident: bib64 article-title: Inhibition of mechanical allodynia in neuropathic pain by TLR5-mediated A-fiber blockade publication-title: Nature Medicine doi: 10.1038/nm.3978 contributor: fullname: Xu – volume: 391 start-page: 390 year: 1998 ident: bib48 article-title: NIP domain prevents N-type inactivation in voltage-gated potassium channels publication-title: Nature doi: 10.1038/34916 contributor: fullname: Roeper – volume: 17 start-page: 153 year: 2014 ident: bib62 article-title: Regulating excitability of peripheral afferents: emerging ion channel targets publication-title: Nature Neuroscience doi: 10.1038/nn.3602 contributor: fullname: Waxman – volume: 14 start-page: 162 year: 2015 ident: bib16 article-title: Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis publication-title: The Lancet. Neurology doi: 10.1016/S1474-4422(14)70251-0 contributor: fullname: Finnerup – volume: 155 start-page: 1272 year: 2014 ident: bib22 article-title: Primary afferent input critical for maintaining spontaneous pain in peripheral neuropathy publication-title: Pain doi: 10.1016/j.pain.2014.03.022 contributor: fullname: Haroutounian – volume: 24 start-page: 1037 year: 1999 ident: bib42 article-title: Caspr2, a new member of the neurexin superfamily, is localized at the juxtaparanodes of myelinated axons and associates with K+ channels publication-title: Neuron doi: 10.1016/S0896-6273(00)81049-1 contributor: fullname: Poliak – volume: 22 start-page: 502 year: 1999 ident: bib25 article-title: Changes in expression of voltage-gated potassium channels in dorsal root ganglion neurons following axotomy publication-title: Muscle & Nerve doi: 10.1002/(SICI)1097-4598(199904)22:4<502::AID-MUS12>3.0.CO;2-K contributor: fullname: Ishikawa – volume: 29 start-page: 3120 year: 2009 ident: bib35 article-title: Variable threshold of trigeminal cold-thermosensitive neurons is determined by a balance between TRPM8 and Kv1 potassium channels publication-title: The Journal of Neuroscience doi: 10.1523/JNEUROSCI.4778-08.2009 contributor: fullname: Madrid – volume: 77 start-page: 899 year: 2013 ident: bib21 article-title: Kv1.1 channels act as mechanical brake in the senses of touch and pain publication-title: Neuron doi: 10.1016/j.neuron.2012.12.035 contributor: fullname: Hao – volume: 30 start-page: 369 year: 2001 ident: bib4 article-title: Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin publication-title: Neuron doi: 10.1016/S0896-6273(01)00294-X contributor: fullname: Bhat – volume: 50 start-page: 1672 year: 1996 ident: bib37 article-title: Novel nonpeptide agents potently block the C-type inactivated conformation of Kv1.3 and suppress T cell activation publication-title: Molecular Pharmacology contributor: fullname: Nguyen – volume: 479 start-page: 424 year: 2004 ident: bib3 article-title: Acute demyelination disrupts the molecular organization of peripheral nervous system nodes publication-title: The Journal of Comparative Neurology doi: 10.1002/cne.20321 contributor: fullname: Arroyo – volume: 3 year: 2014 ident: bib10 article-title: Transcriptional profiling at whole population and single cell levels reveals somatosensory neuron molecular diversity publication-title: eLife doi: 10.7554/eLife.04660 contributor: fullname: Chiu – volume: 340 start-page: 19 year: 1985 ident: bib13 article-title: Peripheral axotomy induces neurofilament decrease, atrophy, demyelination and degeneration of root and fasciculus gracilis fibers publication-title: Brain Research doi: 10.1016/0006-8993(85)90771-1 contributor: fullname: Dyck – volume: 151 start-page: 862 year: 2010 ident: bib54 article-title: Surgical management of neuroma pain: a prospective follow-up study publication-title: Pain doi: 10.1016/j.pain.2010.09.032 contributor: fullname: Stokvis – volume: 59 start-page: 1447 year: 2011 ident: bib53 article-title: Paranodal permeability in "myelin mutants" publication-title: Glia doi: 10.1002/glia.21188 contributor: fullname: Shroff – volume: 134 start-page: 320 year: 2008 ident: bib12 article-title: The tibial neuroma transposition (TNT) model of neuroma pain and hyperalgesia publication-title: Pain doi: 10.1016/j.pain.2007.06.030 contributor: fullname: Dorsi – volume: 73 start-page: 345 year: 1981 ident: bib50 article-title: Development of ongoing activity, mechanosensitivity, and adrenaline sensitivity in severed peripheral nerve axons publication-title: Experimental Neurology doi: 10.1016/0014-4886(81)90271-5 contributor: fullname: Scadding – volume: 85 start-page: 238 year: 2015 ident: bib57 article-title: Subcellular localization of K+ channels in mammalian brain neurons: remarkable precision in the midst of extraordinary complexity publication-title: Neuron doi: 10.1016/j.neuron.2014.12.042 contributor: fullname: Trimmer – volume: 16 start-page: 256 year: 2003 ident: bib40 article-title: Downregulation of voltage-gated potassium channel alpha gene expression by axotomy and neurotrophins in rat dorsal root ganglia publication-title: Molecules and Cells contributor: fullname: Park – volume: 350 start-page: 232 year: 1991 ident: bib34 article-title: Determination of the subunit stoichiometry of a voltage-activated potassium channel publication-title: Nature doi: 10.1038/350232a0 contributor: fullname: MacKinnon – volume: 203 start-page: 437 year: 2013 ident: bib68 article-title: Membrane domain organization of myelinated axons requires βII spectrin publication-title: The Journal of Cell Biology doi: 10.1083/jcb.201308116 contributor: fullname: Zhang – volume: 124 start-page: 222 year: 2006 ident: bib24 article-title: Increased sodium channel immunofluorescence at myelinated and demyelinated sites following an inflammatory and partial axotomy lesion of the rat infraorbital nerve publication-title: Pain doi: 10.1016/j.pain.2006.05.028 contributor: fullname: Henry – volume: 84 start-page: 309 year: 2000 ident: bib33 article-title: Spontaneous activity of axotomized afferent neurons after L5 spinal nerve injury in rats publication-title: Pain doi: 10.1016/S0304-3959(99)00211-0 contributor: fullname: Liu – volume: 30 start-page: 385 year: 2001 ident: bib6 article-title: Contactin orchestrates assembly of the septate-like junctions at the paranode in myelinated peripheral nerve publication-title: Neuron doi: 10.1016/S0896-6273(01)00296-3 contributor: fullname: Boyle – volume: 120 start-page: 24 year: 2006 ident: bib49 article-title: Cold sensitivity in axotomized fibers of experimental neuromas in mice publication-title: Pain doi: 10.1016/j.pain.2005.10.006 contributor: fullname: Roza – volume: 283 start-page: 570 year: 1980 ident: bib52 article-title: Effects of 4-aminopyridine on normal and demyelinated mammalian nerve fibres publication-title: Nature doi: 10.1038/283570a0 contributor: fullname: Sherratt – volume: 19 start-page: 8589 year: 1999 ident: bib1 article-title: Membrane potential oscillations in dorsal root ganglion neurons: role in normal electrogenesis and neuropathic pain publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.19-19-08589.1999 contributor: fullname: Amir – volume: 284 start-page: 170 year: 1980 ident: bib9 article-title: Potassium channels in nodal and internodal axonal membrane of mammalian myelinated fibres publication-title: Nature doi: 10.1038/284170a0 contributor: fullname: Chiu – volume: 162 start-page: 1149 year: 2003 ident: bib44 article-title: Juxtaparanodal clustering of Shaker-like K+ channels in myelinated axons depends on Caspr2 and TAG-1 publication-title: The Journal of Cell Biology doi: 10.1083/jcb.200305018 contributor: fullname: Poliak – volume: 50 start-page: 355 year: 1992 ident: bib29 article-title: An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat publication-title: Pain doi: 10.1016/0304-3959(92)90041-9 contributor: fullname: Kim – volume: 84 start-page: 253 year: 2000 ident: bib20 article-title: Characteristics of ectopic discharges in a rat neuropathic pain model publication-title: Pain doi: 10.1016/S0304-3959(99)00219-5 contributor: fullname: Han – volume: 75 start-page: 2629 year: 1996 ident: bib18 article-title: Characterization of six voltage-gated K+ currents in adult rat sensory neurons publication-title: Journal of Neurophysiology doi: 10.1152/jn.1996.75.6.2629 contributor: fullname: Gold – volume: 105 start-page: 146 year: 2002 ident: bib30 article-title: Downregulation of voltage-gated potassium channel alpha gene expression in dorsal root ganglia following chronic constriction injury of the rat sciatic nerve publication-title: Molecular Brain Research doi: 10.1016/S0169-328X(02)00388-1 contributor: fullname: Kim – volume: 150 start-page: 657 year: 2000 ident: bib55 article-title: An oligodendrocyte cell adhesion molecule at the site of assembly of the paranodal axo-glial junction publication-title: The Journal of Cell Biology doi: 10.1083/jcb.150.3.657 contributor: fullname: Tait – volume: 210 start-page: 51 year: 2008 ident: bib58 article-title: Expression and localization of Kv1 potassium channels in rat dorsal and ventral spinal roots publication-title: Experimental Neurology doi: 10.1016/j.expneurol.2007.09.032 contributor: fullname: Utsunomiya – volume: 19 start-page: 747 year: 1999 ident: bib59 article-title: Dynamic potassium channel distributions during axonal development prevent aberrant firing patterns publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.19-02-00747.1999 contributor: fullname: Vabnick – volume: 98 start-page: 13373 year: 2001 ident: bib47 article-title: Distinct potassium channels on pain-sensing neurons publication-title: Proceedings of the National Academy of Sciences of the United States of America doi: 10.1073/pnas.231376298 contributor: fullname: Rasband – volume: 16 start-page: 1024 year: 2013 ident: bib69 article-title: A long noncoding RNA contributes to neuropathic pain by silencing Kcna2 in primary afferent neurons publication-title: Nature Neuroscience doi: 10.1038/nn.3438 contributor: fullname: Zhao – volume: 25 start-page: 2576 year: 2005 ident: bib2 article-title: Multiple interacting sites of ectopic spike electrogenesis in primary sensory neurons publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.4118-04.2005 contributor: fullname: Amir – volume: 85 start-page: 503 year: 2000 ident: bib32 article-title: Tactile allodynia in the absence of C-fiber activation: altered firing properties of DRG neurons following spinal nerve injury publication-title: Pain doi: 10.1016/S0304-3959(00)00251-7 contributor: fullname: Liu – volume: 7 year: 2014 ident: bib56 article-title: Defining the nociceptor transcriptome publication-title: Frontiers in Molecular Neuroscience doi: 10.3389/fnmol.2014.00087 contributor: fullname: Thakur – volume: 27 start-page: 211 year: 1981 ident: bib39 article-title: Microelectrode recordings from transected nerves in amputees with phantom limb pain publication-title: Neuroscience Letters doi: 10.1016/0304-3940(81)90270-6 contributor: fullname: Nyström – volume: 133 start-page: 389 year: 2010 ident: bib45 article-title: Novel forms of neurofascin 155 in the central nervous system: alterations in paranodal disruption models and multiple sclerosis publication-title: Brain doi: 10.1093/brain/awp341 contributor: fullname: Pomicter – volume: 104 start-page: 20055 year: 2007 ident: bib66 article-title: Trafficking-dependent phosphorylation of Kv1.2 regulates voltage-gated potassium channel cell surface expression publication-title: Proceedings of the National Academy of Sciences of the United States of America doi: 10.1073/pnas.0708574104 contributor: fullname: Yang – volume: 8 start-page: e1000412 year: 2010 ident: bib28 article-title: Improving bioscience research reporting: the ARRIVE guidelines for reporting animal research publication-title: PLoS Biology doi: 10.1371/journal.pbio.1000412 contributor: fullname: Kilkenny – volume: 286 start-page: 25835 year: 2011 ident: bib19 article-title: Clustering and activity tuning of Kv1 channels in myelinated hippocampal axons publication-title: The Journal of Biological Chemistry doi: 10.1074/jbc.M111.219113 contributor: fullname: Gu – volume: 17 start-page: 321 year: 1983 ident: bib61 article-title: Sensory afferent impulses originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats publication-title: Pain doi: 10.1016/0304-3959(83)90164-1 contributor: fullname: Wall – volume: 26 start-page: 788 year: 2010 ident: bib38 article-title: Neuroma removal for neuropathic pain: efficacy and predictive value of lidocaine infusion publication-title: The Clinical Journal of Pain doi: 10.1097/AJP.0b013e3181ed0823 contributor: fullname: Nikolajsen – volume: 290 start-page: 124 year: 2000 ident: bib5 article-title: Potent analgesic effects of GDNF in neuropathic pain states publication-title: Science doi: 10.1126/science.290.5489.124 contributor: fullname: Boucher – volume: 6 start-page: 79 year: 1988 ident: bib17 article-title: End-structure of afferent axons injured in the peripheral and central nervous system publication-title: Somatosensory & Motor Research doi: 10.3109/08990228809144642 contributor: fullname: Fried – volume: 20 start-page: 2742 year: 2000 ident: bib36 article-title: Axotomized and intact muscle afferents but no skin afferents develop ongoing discharges of dorsal root ganglion origin after peripheral nerve lesion publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.20-07-02742.2000 contributor: fullname: Michaelis – volume: 72 start-page: 159 year: 2013 ident: bib8 article-title: Excitable domains of myelinated nerves: axon initial segments and nodes of Ranvier publication-title: Current Topics in Membranes doi: 10.1016/B978-0-12-417027-8.00005-2 contributor: fullname: Chang – volume: 18 start-page: 36 year: 1998 ident: bib46 article-title: Potassium channel distribution, clustering, and function in remyelinating rat axons publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.18-01-00036.1998 contributor: fullname: Rasband – volume: 21 start-page: 7568 year: 2001 ident: bib43 article-title: Localization of Caspr2 in myelinated nerves depends on axon-glia interactions and the generation of barriers along the axon publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.21-19-07568.2001 contributor: fullname: Poliak – volume: 46 start-page: 155 year: 2012 ident: bib31 article-title: The role of sodium channels in chronic pain publication-title: Muscle & Nerve doi: 10.1002/mus.23314 contributor: fullname: Levinson – volume: 21 start-page: RC140 year: 2001 ident: bib63 article-title: Early onset of spontaneous activity in uninjured C-fiber nociceptors after injury to neighboring nerve fibers publication-title: Journal of Neuroscience doi: 10.1523/JNEUROSCI.21-08-j0002.2001 contributor: fullname: Wu – volume: 32 start-page: 89 year: 1988 ident: bib7 article-title: Myelinated afferents signal the hyperalgesia associated with nerve injury publication-title: Pain doi: 10.1016/0304-3959(88)90027-9 contributor: fullname: Campbell – volume: 48 start-page: 737 year: 2005 ident: bib51 article-title: Neurofascins are required to establish axonal domains for saltatory conduction publication-title: Neuron doi: 10.1016/j.neuron.2005.10.019 contributor: fullname: Sherman – volume: 39 start-page: 15 year: 2001 ident: bib23 article-title: Twenty years of dendrotoxins publication-title: Toxicon doi: 10.1016/S0041-0101(00)00162-8 contributor: fullname: Harvey – volume: 590 start-page: 2591 year: 2012 ident: bib26 article-title: Voltage-gated potassium channels and the diversity of electrical signalling publication-title: The Journal of Physiology doi: 10.1113/jphysiol.2011.224212 contributor: fullname: Jan – volume: 248 start-page: 740 year: 1974 ident: bib60 article-title: Properties of afferent nerve impulses originating from a neuroma publication-title: Nature doi: 10.1038/248740a0 contributor: fullname: Wall |
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| Snippet | Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over... |
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| SubjectTerms | Action Potentials Animals Axons Axons - physiology Health aspects Humans hypersensitivity juxtaparanode Localization Neural circuitry Neurons neuropathic pain neuropathy Neuroscience Pain Peripheral nerve diseases Peripheral Nerve Injuries - physiopathology Peripheral neuropathy Potassium channels Potassium channels (voltage-gated) Prevention Rats Rodents Sensory neurons Shaker Superfamily of Potassium Channels - metabolism shaker type potassium channels |
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| Title | Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury |
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